Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental contaminants whose metabolism in mammals results in deleterious cell transformation. Covalently modification of DNA by diol epoxides metabolically formed from PAHs such as benzo[a]pyrene (BaP) provides a mechanism for the genotoxicity, mutagenicity, and carcinogenicity of PAHs. Using 2D NMR spectroscopy and molecular modeling we continue to investigate solution structures of DNA duplexes containing a dA residue modified at the exocyclic amino group by trans (or cis) addition to C-10 isomeric 7,8-diol 9,10-epoxide metabolites of benzo[a]pyrene (BPDEs). We have previously reported the solution structure for a major conformer of the duplex d(G1G2T3C4A5*C6G7A8G9).d(C10T11C12G13G14G15A16C17C18) containing a dG14 mismatch opposite a dA5* residue modified at the exocyclic amino group by trans addition to (+)-(7R,8S,9S,10R)-7,8-dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[ a]pyrene. The structure of a minor conformer of this carcinogen-lesion DNA adduct now is determined. The major structural differences between the two conformers appears to be near the lesion site as evidenced by the large chemical shift differences between major and minor conformer protons near the lesion site. In the minor conformer, the adducted base assumes an anti-glycosidic torsion angle whereas in the major conformer it assumes an unusual syn-glycosidic torsion angle. We are also conducting spectral assignments and structural analysis of DNA duplexes containing other dA-BP adducts. Enzyme digestion and chemical reduction of fungal cell walls yielded a number of soluble high molecular weight materials. Four major structural components of the cell wall were identified by 1H and 13C NMR spectroscopy as b(1-3)-glucan, b(1-6)-glucan, chitin and mannoprotein. We found that these four components are covalently linked together, which may explain the strength and resilience of the fungal cell wall. The mechanism of biosynthesis of the cross-linkage awaits further work.